Evidence map›Paper›PMID 28825683›Full record

ReviewInternational journal of molecular sciences2017

Towards a Better Understanding of GABAergic Remodeling in Alzheimer's Disease.

Karan Govindpani, Beatriz Calvo-Flores Guzmán, Chitra Vinnakota, Henry J Waldvogel, Richard L Faull, Andrea Kwakowsky

Abstract readReview
In one paragraph

Review in International journal of molecular sciences, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 99 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
99citing papers in PubMed, 1 pooled it
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

99 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Article
  3. Neurotransmitter Systems in Alzheimer's Disease.Current issues in molecular biology · 2026
    Review
  4. Article
  5. Article
  6. Article
  7. Review
  8. Review
  9. Beyond epilepsy: The expanding role of valproic acid in Alzheimer disease therapy - a review.The Journal of pharmacology and experimental therapeutics · 2025
    Review
  10. Article
  11. Article
  12. The function of chloride channels in digestive system disease (Review).International journal of molecular medicine · 2025
    Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. Regulation of Hippocamposeptal Synaptic Transmission by GABAJournal of molecular neuroscience : MN · 2024
    Article
  20. Article

39 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors.

Karan GovindpaniCentre for Brain Research, Department of Anatomy and Medical Imaging, Faculty of Medical and Health Sciences, University of Auckland, Auckland 1023, New Zealand. k.govindpani@auckland.ac.nz.
Beatriz Calvo-Flores GuzmánCentre for Brain Research, Department of Anatomy and Medical Imaging, Faculty of Medical and Health Sciences, University of Auckland, Auckland 1023, New Zealand. b.guzman@auckland.ac.nz.
Chitra VinnakotaCentre for Brain Research, Department of Anatomy and Medical Imaging, Faculty of Medical and Health Sciences, University of Auckland, Auckland 1023, New Zealand. c.vinnakota@auckland.ac.nz.
Henry J WaldvogelCentre for Brain Research, Department of Anatomy and Medical Imaging, Faculty of Medical and Health Sciences, University of Auckland, Auckland 1023, New Zealand. h.waldvogel@auckland.ac.nz.
Richard L FaullCentre for Brain Research, Department of Anatomy and Medical Imaging, Faculty of Medical and Health Sciences, University of Auckland, Auckland 1023, New Zealand. rlm.faull@auckland.ac.nz.
Andrea KwakowskyCentre for Brain Research, Department of Anatomy and Medical Imaging, Faculty of Medical and Health Sciences, University of Auckland, Auckland 1023, New Zealand. a.kwakowsky@auckalnd.ac.nz.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

γ-aminobutyric acid (GABA) is the primary inhibitory neurotransmitter in the vertebrate brain. In the past, there has been a major research drive focused on the dysfunction of the glutamatergic and cholinergic neurotransmitter systems in Alzheimer's disease (AD). However, there is now growing evidence in support of a GABAergic contribution to the pathogenesis of this neurodegenerative disease. Previous studies paint a complex, convoluted and often inconsistent picture of AD-associated GABAergic remodeling. Given the importance of the GABAergic system in neuronal function and homeostasis, in the maintenance of the excitatory/inhibitory balance, and in the processes of learning and memory, such changes in GABAergic function could be an important factor in both early and later stages of AD pathogenesis. Given the limited scope of currently available therapies in modifying the course of the disease, a better understanding of GABAergic remodeling in AD could open up innovative and novel therapeutic opportunities.

Indexed as

Alzheimer DiseaseBrainGABAergic Neuronsgamma-Aminobutyric AcidHumansNeurotransmitter Agentsgamma-Aminobutyric AcidNeurotransmitter AgentsAlzheimer’s diseaseE/I balanceGABAGABA receptorGABA transporterGADGAT

Identifiers

PMID28825683
PMCPMC5578199

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.